This paper aims to explore the relationship of retinal neuron apoptosis and manganese superoxidase dismutase (MnSOD) at early phase of diabetic retinopathy. Sprague-Dawley rats were grouped into normal controls and diabetics. Data were collected after 4, 8, and 12 weeks ( ). The pathological changes and ultrastructure of the retina, the apoptosis rate of retinal neurons by TdT-mediated dUTP nick end label (TUNEL), mRNA expressions of MnSOD and copper-zinc superoxide dismutase (Cu–Zn SOD), and the activities of total SOD (T-SOD) and subtypes of SOD were tested. For the controls, there was no abnormal structure or apoptosis of retinal neurons at any time. There was no change of structure for rats with diabetes at 4 or 8 weeks, but there was a decrease of retinal ganglion cells (RGCs) number and thinner inner nuclear layer (INL) at 12 weeks. The apoptosis ratio of RGCs was higher than that of the controls at 8 and 12 weeks ( ). The activity and mRNA levels of MnSOD were lower in diabetics at 4, 8, and 12 weeks ( ). In summary, the apoptosis of the retinal neurons occurred at 8 weeks after the onset of diabetes. Retinal neuron apoptosis in early diabetic rats may be associated with the decreased activity and mRNA of MnSOD. 1. Introduction Diabetic retinopathy (DR) is a chronic complication of diabetes mellitus (DM), the leading cause of blindness in adults, affecting 51 million people all over the world [1, 2]. The prevalence of diabetic retinopathy is about 20.5%~46.9% [3, 4]. DR is not just a microvascular complication of DM [5–7]. All types of cells within the retina are involved in an array of pathophysiological processes even at the early stages of diabetes. A growing number of studies suggested that DR is also the lesion of the retinal neurons [8, 9]. The newly onset clinical features of DR, breakdown of the blood-retinal barrier (BRB), and various visual deficits all support this concept in human studies [10–13]. Because of gradual and accelerating deterioration, intervention should be implemented before irreversible DR occurs [14, 15]. Although the mechanism remains unclear, it is generally believed that excessive reactive oxygen species (ROS) from mitochondria induce apoptosis. With the consequent oxidative damages, it contributed to the development of diabetes and DR [16–19]. The importance of mitochondria in regulating apoptosis has been well documented. Under hyperglycemic conditions, inflammation [20] and excessive ROS damage mitochondria and thus promote the release of apoptosis-inducing factors such as cytochrome C, which further activates
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